Pre-excitation syndrome: Difference between revisions

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==Historical Perspective==
==Historical Perspective==
*In 1915, [[Frank Norman Wilson]] became the first to describe the [[condition]] which would later be referred to as [[Wolff–Parkinson–White syndrome]].
*In 1915, [[Frank Norman Wilson]] became the first to describe the [[condition]] which would later be referred to as [[Wolff–Parkinson–White syndrome]].
*In 1930, [[WPW syndrome]] was first described and named after [[John Parkinson]], [[Paul Dudley White]], and [[Louis Wolff]]. They successfully interpreted a series of 11 [[healthy]] young [[patients]] who had repeated attacks of [[tachycardia]] in the presence of [[short PR interval]] and [[bundle branch block]] pattern on the [[ECG]] findings. They also found the [[Association (statistics)|association]] of [[WPW]] with increasing the [[risk]] of [[sudden cardiac death]].
*In 1930, [[WPW syndrome]] was first described and named after [[John Parkinson]], [[Paul Dudley White]], and [[Louis Wolff]]. They successfully interpreted a series of 11 [[healthy]] young [[patients]] who had repeated attacks of [[tachycardia]] in the presence of [[short PR interval]] and [[bundle branch block]] pattern on the [[ECG]] findings. They also found the [[Association (statistics)|association]] of [[WPW]] with increasing the [[risk]] of [[sudden cardiac death]].
*British physiologist "Albert Frank Stanley Kent" (1863 - 1958), first described the lateral branches of [[AV grove]] of the [[monkey]] [[heart]], which was later named accessory [[bundle of Kent]].
*British physiologist "Albert Frank Stanley Kent" (1863 - 1958), first described the lateral branches of [[AV grove]] of the [[monkey]] [[heart]], which were later named as the <nowiki>''</nowiki>accessory [[bundle of Kent]]<nowiki>''</nowiki>.


[[File:Wolf-parkinson-white.jpg|thumb|300px|none|WPW Syndrome was given its name in 1930 by Wolf, Parkinson, and White. [https://en.ecgpedia.org/index.php?title=File:Wolffparkinsonwhite.jpg Source: Ecgpedia.org]]]
[[File:Wolf-parkinson-white.jpg|thumb|300px|none|WPW Syndrome was given its name in 1930 by Wolf, Parkinson, and White. [https://en.ecgpedia.org/index.php?title=File:Wolffparkinsonwhite.jpg Source: Ecgpedia.org]]]
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*Based on their [[conduction]] properties, three types of [[accessory pathways]] are there:
*Based on their [[conduction]] properties, three types of [[accessory pathways]] are there:
#[[Accessory pathway|Manifest Accessory Pathways]]: [[Conducts]] more rapidly as compared to [[AV nodal conduction]]. [[Delta waves]] will commonly be seen on [[ECG]].
#[[Accessory pathway|Manifest Accessory Pathways]]: [[Conducts]] more rapidly as compared to [[AV nodal conduction]]. [[Delta waves]] will commonly be seen on [[ECG]].
#[[Concealed]] [[Accessory Pathways]]: [[Conducts]] in the [[retrograde direction]]. As its name represents, the changes in [[ECG]] will be [[concealed]]. No [[delta waves]] will be seen.
#[[Concealed]] [[Accessory Pathways]]: [[Conducts]] in the [[retrograde direction]]. As its name represents, the changes in [[ECG]] will be [[concealed]]. No [[delta waves]] will be seen.

Revision as of 17:08, 24 September 2020

Pre-excitation syndrome Microchapters

Overview

Historical Perspective

Classification

Pathophysiology

Differentiating Pre-excitation Syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications, and Prognosis

Diagnosis

Treatment

Prevention

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2] Associate Editor(s)-in-Chief: Shivam Singla, M.D.[3]

Synonyms and keywords: Pre Excitation Syndromes; Lown-Ganong-Levine Syndrome; Pre-Excitation, Mahaim-Type; Wolff-Parkinson-White Syndrome

Overview

Pre-excitation syndrome is a condition where ventricles of the heart depolarize earlier than expected via some accessory pathway conduction hence, leading to the premature contraction. Normally the atria and the ventricles are interconnected through the AV node (atrioventricular node). But in all the pre-excitation syndromes, an accessory pathway is present that conducts impulses to ventricles besides the AV node. The accessory pathway passes the electrical impulses to the ventricles before the normal impulse of depolarization passes through the AV node. The phenomenon of depolarizing ventricles through the accessory pathway earlier than the usual depolarization is supposed to happen through the AV node is referred to as "Pre- Excitation". WPW syndrome was described in 1930 and named after John Parkinson, Paul Dudley White, and Louis Wolff. The accessory pathways are named depending upon the regions of atria and ventricles they are connecting such as Bundle of His, Mahaim fibers, and James fibers.

The typical ECG findings associated with WPW syndrome are shortened PR interval, widened QRS complex and Delta wave which is a slurring in the upstroke of QRS complex due to preexcitation of ventricles via the accessory pathway. ECG findings along with symptomatic tachyarrhythmias are referred to as Wolff-Parkinson-White syndrome. Although it is more common in the adult, males have an incidence rate of 0.1-0.3 %, WPW can be considered as a congenital anomaly in some cases where it is usually present since the birth and in others, it is considered as a developmental anomaly. Studies have proven its lower prevalence in children aged between 6-13 than those in the age group of 14-15 years of age. Hemodynamically unstable patients should be managed with a direct cardioversion. For the stable patients, medical management should be tried first before going for other acceptable options of catheter ablation or surgical intervention. Although Catheter ablation has widely replaced the surgical option due to its less invasive technique and better outcomes, still in cases where catheter ablation cannot be done or doesn't prove to be effective, the surgical option is worth considering with a curative rate of nearly 100%.

Historical Perspective

WPW Syndrome was given its name in 1930 by Wolf, Parkinson, and White. Source: Ecgpedia.org

Classification

Type Conduction pathway QRS interval PR interval Delta wave
Wolff-Parkinson-White syndrome Bundle of Kent Wide/long Usually short Yes
Lown-Ganong-Levine syndrome "James bundle" (atria to bundle of His) Normal/Unaffected Short No
Mahaim-type Mahaim fibers Long Normal No
  1. Manifest Accessory Pathways: Conducts more rapidly as compared to AV nodal conduction. Delta waves will commonly be seen on ECG.
  2. Concealed Accessory Pathways: Conducts in the retrograde direction. As its name represents, the changes in ECG will be concealed. No delta waves will be seen.
  3. Latent Accessory Pathways: These are located in the lateral part of the heart as compared to AV node. So the impulses will be delayed in traveling to ventricles through the AV node which is at a much shorter distance as compared to latent fibers that are at the far another end.

Pathophysiology

Differentiating Pre-excitation Syndrome from other Diseases

Arrhythmia Rhythm Rate P wave PR Interval QRS Complex Response to Maneuvers Epidemiology Co-existing Conditions
Atrial Fibrillation (AFib)
  • Absent
  • Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction
  • 2.7–6.1 million people in the United States have AFib
  • 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib
Atrial Flutter
  • 75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common
  • Varies depending upon the magnitude of the block, but is short
  • Less than 0.12 seconds, consistent, and normal in morphology
  • Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
Atrioventricular nodal reentry tachycardia (AVNRT)''''
  • 140-280 bpm
Multifocal Atrial Tachycardia
  • Irregular
  • Atrial rate is > 100 beats per minute
  • Less than 0.12 seconds, consistent, and normal in morphology
Paroxysmal Supraventricular Tachycardia
  • Regular
  • 150 and 240 bpm
  • Absent
  • Hidden in QRS
  • Absent
  • Narrow complexes (< 0.12 s)
Premature Atrial Contractrions (PAC)
  • 80-120 bpm
  • Upright
  • Usually narrow (< 0.12 s)
Wolff-Parkinson-White Syndrome
  • Regular
  • Atrial rate is nearly 300 bpm and the ventricular rate is at 150 bpm
  • Less than 0.12 seconds
Ventricular Fibrillation (VF)
  • Irregular
  • 150 to 500 bpm
  • Absent
  • Absent
  • Absent (R on T phenomenon in the setting of ischemia)
Ventricular Tachycardia
  • Regular
  • > 100 bpm (150-200 bpm common)
  • Absent
  • Absent
  • Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation
  • Wide complex, QRS duration > 120 milliseconds
  • 5-10% of patients presenting with AMI

Epidemiology and Demographics

Risk Factors

High-risk population for development of atrial fibrillation or sudden cardiac death include:

Natural History, Complications, and Prognosis

Natural History

Complications

Prognosis

Diagnosis

WPW Syndrome

WPW ECG changes with significant 1) Delta wave 2) PR interval shortening 3) Wide QRS complexes. [1]

Lown-Ganong-Levine(LGL) Syndrome

Mahaim-Type Pre-excitation

History and Symptoms

Treatment

Medical Treatment

HEMODYNAMICALY UNSTABLE PATIENT -- DIRECT SYNCHRONIZED CARDIOVERSION, BIPHASIC ( INITIAL 100 J, LATER ON- 200J OR 360J).

HEMODYNAMICALLY STABLE PATIENTS -- THE FOLLOWING ALGORITHM CAN BE FOLLOWED

GENERAL PROTOCOL

IN CASE OF ACUTE AVRT/AVNRT

ATRIAL FLUTTER/FIBRILLATION

RADIOFREQUENCY ABLATION

Class 3 Antiarrhythmics and class IC drugs are used with AV nodal blocking agents in patients with a history of atrial flutter or A.Fib. Sotalol and Flecainide would be the safe options to use in pregnancy.

Surgical management

Prevention

References